In patients with coronary artery disease, a critical reduction in blood flow has been proposed as the mechanism responsible for chronic left ventricular dysfunction. To test this hypothesis, we have investigated the relation between the effect of coronary stenoses on resting systolic function and on myocardial contractile reserve during adrenergic stimulation using a quantitative assessment of myocardial contraction. If a reduction in blood flow accounted for the diminished myocardial performance, then the magnitude of impairement of systolic function at rest would be related to the inotropic response to dobutamine. Instead, our results demonstrated that there is no correlation between basal and stimulated myocardial contraction, suggesting that limitation of blood flow is unlikely to be the sole mechanism responsible for chronic left ventricular dysfunction in coronary artery disease. To assess whether patients with chest pain despite normal coronary arteriograms have mild degree of ischemia as the cause of their symptoms, we analyzed the quantitative myocardial contractile response to dobutamine. No difference was observed between patients and normal controls. These findings strongly suggest that myocardial ischemia is not responsible for the chest pain symptoms referred to by these patients and support the concept of abnormal cardiac nociception in this condition. In patients with chronic severe aortic regurgitation and normal left ventricular function, valve replacement is not recommended until symptoms, left ventricular dysfunction or progressive dilatation develop during follow-up. However, whether concealed myocardial dysfunction can occur before those obvious indices of deterioration are detected has not been established. Using dobutamine echocardiography, we found that, compared to normal controls, patients with aortic regurgitation have markedly reduced inotropic reserve, which is not related to the magnitude of afterload changes and may represent an early stage of myocardial dysfunction in some patients.